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Adverse reactions to foods are classified into 3 categories: food anaphylaxis, food hypersensitivity, and food intolerance. Anaphylaxis and hypersensitivity involve allergic mechanisms, whereas intolerance is a reproducible nonallergic response. Allergic food reactions may be broadly divided into immunoglobulin (Ig) E–mediated (eg, anaphylaxis) or non–IgE-mediated (eg, celiac). Food anaphylaxis is an IgE-mediated reaction of rapid onset (within minutes) and includes classic anaphylaxis and oral allergy syndrome. Food hypersensitivity includes immunologic reactions that are typically delayed and cell-mediated with or without IgE antibody involvement including food protein-induced enterocolitis syndrome (FPIES), food protein-induced proctocolitis, and celiac disease. Food intolerance represents an abnormal, nonallergic physiologic response including idiosyncratic (monosodium glutamate), metabolic (galactosemia), digestive (lactase deficiency), pharmacologic (caffeine), toxic (Bacillus cereus), organ based (irritable bowel syndrome), or behavioral (food texture aversion) reactions. Food allergic gastroenteropathies are characterized by common gastrointestinal (GI) symptoms that occur with ingestion of food allergens. The 2 most common allergic GI diseases are allergic proctocolitis (AC) and FPIES. Since the clinical phenotype of patients with AC and FPIES are so distinct, GI mucosal biopsies are typically not necessary to make these diagnoses.

Eosinophilic GI diseases (EGIDs) are a heterogeneous group of diseases that are characterized by a range of symptoms that reflect the part of the GI tract that is inflamed. For instance, a highly atopic teenager who presents with food impaction will likely have eosinophilic esophagitis (EoE), and a nonatopic child who presents with vague symptoms such as abdominal pain, peripheral eosinophilia, and stomach ulcers may have eosinophilic gastritis (EG). One factor contributing to some of the slow progress in understanding EGIDs is the fact that eosinophils are normal constituents of the GI tract, raising the possibility that they contribute to both host defense and disease states. For example, increased numbers of mucosal eosinophilia can be found during parasitic, bacterial, and viral infections as well as certain systemic diseases such as vasculitis and inflammatory bowel disease.

Collectively, allergic gastroenteropathies and EGIDs are presented together here because food allergens likely serve as triggers for their underlying pathogenesis (Table 406-1). With respect to allergic gastroenteropathies, clinical evidence provides strong evidence for food as an underlying cause. For EGIDs, less is known, but certainly for EoE, foods may be an instigating factor.


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